Drug Database
AD

AD-201 (AD 201 / AD201)

✓ Approved

Addpharma · Small Molecule · Small Molecule

What is AD-201?

AD-201 is a small molecule developed by Addpharma. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesAD 201, AD201
CompanyAddpharma
Drug ClassSmall Molecule
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, Addpharma

Therapeutic Indications

AD-201 is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved
Metabolism and nutrition disordersHyperlipidaemia✓ Approved

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PubMediScience2026-08-30

Comparative effectiveness of multiple interventions for Alzheimer's disease on ABC syndromes and QoL: A Bayesian network meta-analysis.

Gao Fujia F, Luo Guangxin G, Liu Bokuan B, Qiu Xu X et al.

Evidence comparing directly pharmacological and non-pharmacological treatments for Alzheimer's disease (AD) is scarce. The ABC symptoms-activities of daily living (ADLs) (A), behavioral and psychological symptoms (BPSs) (B), cognitive function (C), and quality of life (QoL)-are critical for diagnosing and assessing treatment effects in AD. This study aims to evaluate five interventions for AD: pharmacological therapy (PT), photobiomodulation (PBM), cognitive therapy (CT), exercise therapy (ET), and repetitive transcranial magnetic stimulation (rTMS) using a Bayesian network meta-analysis approach. Among 6,450 records screened, 91 randomized controlled trials (RCTs) involving 12,242 participants met the inclusion criteria. PBM and rTMS showed significant benefits for cognitive function in AD patients. PT and CT showed notable effectiveness in enhancing activities of daily living. For QoL, CT and ET were identified as more favorable outcomes. Collectively, each intervention exerts unique merits targeting ABC symptoms and QoL, implying combined pharmacological and non-pharmacological regimens could optimize therapeutic gains for AD management.

PMID 42668611
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PubMedCNS neuroscience & therapeutics2026-08-30

Modulating the Gut-Microbiota-Brain Axis in Alzheimer's Disease: Therapeutic Potential of Nutritional and Metabolic Factors.

Xu Binyue B, Li Xuhuan X, Dong Shangling S, Zhang Zheyuan Z et al.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia among the elderly, characterized by a gradual decline in memory and cognitive function. The growing body of evidence highlighting the interaction between the gut microbiota and the central nervous system has positioned the gut microbiota as a key area of research in AD pathogenesis. This review critically evaluates the preclinical evidence and clinical trial outcomes, complemented by mechanistic studies and Mendelian randomization analyses, to assess the therapeutic potential of nutritional interventions targeting the gut-microbiota-brain axis in AD. Dietary components and patterns regulate the composition and function of the gut microbiota, which in turn influence brain function through the gut-microbiota-brain axis via chemical/metabolic, immune-mediated, and neural pathways. Specific nutrients, microbial metabolites, and dietary patterns have been shown to exert either protective or detrimental effects on AD pathology and cognitive function. Emerging strategies, including precision nutrition, fecal microbiota transplantation, and next-generation microbiome-based therapies, offer new avenues for AD prevention and treatment. Nutritional interventions targeting the gut-microbiota-brain axis represent a promising approach for the comprehensive prevention and management of AD. Further mechanistic and clinical studies are warranted to translate these findings into effective therapeutic strategies.

PMID 42669137
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PubMedJournal of orthopaedic translation2026-08-30

ADSC-derived mitochondrial nanovesicles transplantation alleviates capsular fibrosis and inflammation and improves joint mobility in a rat model of adhesive capsulitis.

Zhu Yiming Y, Wang Zeyu Z, Huo Ziqi Z, Zhang Dan D et al.

Adhesive capsulitis (frozen shoulder) is a prevalent condition characterized by shoulder pain and progressive motion loss. Mitochondrial metabolic dysregulation is an underlying driver of chronic inflammation and fibrosis. This study aimed to characterize mitochondrial metabolic abnormalities in patient capsular tissue and evaluate a therapy using adipose-derived stem cell (ADSC) derived mitochondrial nanovesicles transplantation. Single-cell RNA sequencing was utilized to analyze the expression of nuclear-encoded genes related to mitochondrial metabolism in fibroblast subpopulations from human adhesive capsulitis capsular tissue. ADSC-derived membranes were extruded together with exogenous mitochondria to generate engineered mitochondrial nanovesicles (AD-Mito-NPs). An inflammatory fibroblast model was employed to assess the uptake of AD-Mito-NPs, along with associated transcriptomic and metabolomic changes, and their effects on apoptosis, inflammation, and extracellular matrix (ECM) remodeling. Finally, AD-Mito-NPs were locally injected into a rat model to evaluate joint movement and histopathology. AD-Mito-NPs retained intact respiratory function, high fibroblast internalization efficiency, and stable physicochemical properties for up to 7 days. In vitro inflammatory models verified that AD-Mito-NPs reversed IL-1β-triggered mitochondrial injury and strengthened mitochondrial oxidative phosphorylation. Furthermore, AD-Mito-NPs alleviated intracellular reactive oxygen species accumulation and fibroblast apoptosis, mitigated inflammatory responses, and remodeled extracellular matrix homeostasis. In vivo, intra-articular administration of AD-Mito-NPs improved shoulder joint mobility, attenuated capsular thickening and disordered collagen arrangement, and suppressed local inflammation in a rat model of adhesive capsulitis. Mitochondrial metabolic imbalance is a factor driving capsular fibrosis in adhesive capsulitis. Engineered mitochondrial transplantation offers therapeutic benefits by enhancing mitochondrial energy production, mitigating oxidative stress and inflammation, and restoring ECM balance. This article identifies mitochondrial metabolic dysregulation as a key driver of adhesive capsulitis-related capsular fibrosis and demonstrates that engineered AD-Mito-NPs are a safe platform for clinical translation. These NPs effectively enhance energy metabolism, reduce inflammation, and improve shoulder mobility in models, providing a promising alternative to existing treatments.

PMID 42668640
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PubMedMolecular neurobiology2026-08-30

Promoting Effect of (+)-Borneol on Alzheimer's Disease Treatment in APP Transgenic Zebrafish and Its Blood-Brain Barrier Permeation Mechanism.

Han Zhe Z, Chen Hongsong H, Yao Yuehua Y, Bo Xinru X et al.

( +)-Borneol (Bor) has been shown to enhance drug penetration across the blood-brain barrier (BBB); yet its mechanisms of action and adjuvant effects on Alzheimer's disease (AD) drugs remain insufficiently investigated. This study systematically explored the adjuvant effects of Bor and its underlying mechanisms by employing AB wild-type zebrafish and APP transgenic zebrafish models. Results demonstrated that Bor at concentrations of 0.05 mM or lower exhibited no toxicity toward AB wild-type zebrafish, whereas 0.01 and 0.05 mM Bor significantly increased the expression of green fluorescent protein (GFP) in the zebrafish brain. Genetic analyses revealed that Bor downregulated genes encoding tight junction proteins and P-glycoprotein (P-gp). Drug treatment experiments showed that Bor enhanced the efficacy of AD therapeutic agents, including Zhenbaopill (ZBP, a traditional medicinal preparation) and the synthetic drug 8e. Specifically, Bor ameliorated AD-related behavioral impairments, inhibited cerebral apoptosis, restored the expression of AD-associated genes, normalized the activities of acetylcholine (ACh)-related enzymes, and downregulated both the mRNA and protein levels of Claudin 5. In summary, Bor enhances BBB permeability by regulating the expression of genes encoding BBB-related proteins, thereby increasing the brain concentration and bioavailability of AD drugs with anticholinesterase activity. An appropriate dose of Bor may thus contribute to enhancing the therapeutic efficacy of AD drugs.

PMID 42668348
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PubMedPediatric investigation2026-08-30

Atopic dermatitis and attention-deficit/hyperactivity disorder comorbidity in children and adolescents: Epidemiology, mechanisms, and clinical management.

Zhao Qingyang Q, Liang Yuan Y, Liu Ying Y, Shen Chunping C et al.

Atopic dermatitis (AD) and attention-deficit/hyperactivity disorder (ADHD) frequently co-occur in children and adolescents, increasing the disease burden and clinical complexity. Accumulating evidence suggests that children with AD have a higher risk of incident ADHD, a risk that is particularly pronounced in those with early-onset, severe AD, or significant sleep disturbances. The underlying mechanisms are hypothesized to involve the dysregulation of the "inflammation-itching-neurobehavioral" axis. This narrative review synthesizes current evidence regarding the epidemiology, potential mechanisms, and clinical management of this comorbidity. We propose that proactive screening and aggressive control of skin inflammation and pruritus are key to disrupting this vicious cycle.

PMID 42668711
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PubMedAlzheimer's & dementia : the journal of the Alzheimer's Association2026-08-30

Extracellular matrix remodeling upregulates hippocampal neurogenic niche stiffness and impairs neurogenesis in Alzheimer's disease.

Sun Weiqi W, Yang Biyu B, Zheng Hanyuan H, Wang Qi Q et al.

Preserving adult hippocampal neurogenesis alleviates cognitive deficits in Alzheimer's disease (AD), yet how biophysical alterations in such as stiffness in the neurogenic niche regulate neurogenesis remains unclear. Stiffness in the hippocampal dentate gyrus subgranular cell zone (SGZ) of 5×FAD mice was measured using atomic force microscopy. Extracellular matrix (ECM) components in mice and AD patients were profiled through proteomics. Hydrogels were supplemented in the SGZ to upregulate local stiffness in wildtype mice, while glycosaminoglycanases was injected to downregulated stiffness in 5×FAD mice. Gene expression in the neurogenic lineage was analyzed through single nucleus sequencing. Conditional knockdown or overexpression of mechanosensors and/or Yes-associated protein 1 (YAP1) were achieved using viral vectors. We found SGZ stiffening occured early in 3-month 5×FAD mice, associating with ECM remodeling and neurogenesis impairment. Upregulation of tissue stiffness in the SGZ of wild-type mice via supplementing high-density hydrogel suppressed neurogenesis, whereas downregulaion of the niche stiffness in AD mice using hyaluronidase-1 (HAase1) and other glycosaminoglycanases preserved neurogenesis. Single-nucleus transcriptomics reveals that the HAase1 treatment reshaped transcriptome of the neural stem cells (NSCs) lineage. Specifically, we found that the integrin-YAP1 mechanotransduction axis played important roles in the stiffness-induced neurogenesis deficits. Conditional knockdown of both integrin β1 and YAP in the NSC lineage mitigated stiffness-induced deficits. Consistently, the association of ECM remodeling and neurogenesis impairments were also observed in post mortem AD patients. ECM stiffness plays as a critical regulator of hippocampal neurogenesis, providing potential targets for pro-neurogenic therapeutics of AD.

PMID 42669622
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